کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10158430 | 1666526 | 2018 | 26 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MicroRNA-17 impairs glucose metabolism in insulin-resistant skeletal muscle via repressing glucose transporter 4 expression
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
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چکیده انگلیسی
Elimination of glucose transporter 4 (GLUT4) inevitably induces insulin resistance (IR), aggravating inflammation- and oxidative stress-related disorders. However, the underlying molecular mechanisms remain incompletely understood. In this study, we identified miR-17 as an important regulator of IR by targeting GLUT4. MiR-17 expression was found significantly elevated in skeletal tissues of rats with type 2 diabetes mellitus (T2DM), along with marked downregulation of GLUT4 protein level. Luciferase reporter gene assay demonstrated a direct interaction between miR-17 and the 3'untranslated region of GLUT4 mRNA. Correlation analyses (Spearman, Pearson, and Kendall) revealed that miR-17 level was negatively correlated with GLUT4 expression. Additionally, loss- and gain-of-function analyses showed that overexpression of miR-17 impaired glucose metabolism in L6 rat skeletal muscle cell line. In contrast, knockdown of endogenous miR-17 ameliorated glucose metabolism, accompanied by elevation of GLUT4 protein level. These findings unraveled a novel mechanism for IR that involves repression of GLUT4 by miR-17 and suggested miR-17 as a potential molecular target for the development of new therapeutic approaches for the treatment of T2DM.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 838, 5 November 2018, Pages 170-176
Journal: European Journal of Pharmacology - Volume 838, 5 November 2018, Pages 170-176
نویسندگان
Dan Xiao, Tong Zhou, Yujie Fu, Rui Wang, Haiying Zhang, Mingqi Li, Yuan Lin, Zhange Li, Chaoqian Xu, Baofeng Yang, Ying Zhang, Yong Zhang,